CD34 and myeloproliferative disorder: These preclinical results suggested that plitidepsin had the potentiality to improve the MF phenotype of GATA-1low mice, justifying further clinical development.25 In the current study, we produce evidence that plitidepsin at low nanomolar concentrations exerted potent antiproliferative activity and induced cell cycle arrest and apoptosis in different cellular models of JAK2V617F mutation and also prevented colony formation by primary myeloproliferative neoplasm CD34+ cells.